The major emphasis of this research program will be focused on the ocular physiology of the teleost. Prior experiments in our laboratory have shown that the teleost retina which is normally exposed to PO2 in excess of 900 torr, shows no symptoms of oxygen toxicity when exposed to hyperbaric oxygen (HBO) while frog retinas, normally exposed to PO2s no greater than 60 torr, exhibit O2 toxicity when exposed to HBO. Ocular oxygen toxicity has been defined as the attenuation of the electroretinogram. In the proposed work we will utilize intracellular recordings of resting membrane potentials and transmembrane electrical activity following photostimulation, thus enabling us to identify the particular retinal cells afffected by O2 toxicity. Measurements of Na-K-Mg ATPase activity following HBO exposure will give inforation regarding the susceptibility of this enzyme to oxygen and will clarify its role in O2 toxicity. It is generally assumed that cellular O2 toxicity is mediated through the formation of O2- which in normal tissues can be dismutated by superoxide dismutase (SOD). A comparative study of the distribution of SOD as it related to oxygen partial pressure and oxidative metabolism of retinal tissue will allow us to speculate on the importance of this enzyme in protection against O2 toxicity. In order to correlate the Na-K-Mg- ATPase and SOD data, precise intraretinal oxygen profiles will have to be determined. To further verify the role of SOD as a protective agent aginst O2 toxicity studies on enzyme induction in retinal tissue following HBO will be undertaken.